J Immunol 2011,
PMID: 21911606
Buckley, Julliette M; Liu, Jing Hua; Li, Chong Hui; Blankson, Siobhan; Wu, Qiong Di; Jiang, Yong; Redmond, H Paul; Wang, Jiang Huai
ST2, a member of the Toll/IL-1R superfamily, negatively regulates both TLR2 and TLR4 signaling. In this study, we report that ST2-deficient mice were more susceptible to polymicrobial sepsis than their wild-type littermates, with increased production of proinflammatory cytokines. Bacterial clearance from the circulation and visceral organs following polymicrobial infection was markedly impaired in ST2-deficient mice. This was associated with substantially reduced uptake, phagocytosis, and intracellular killing of both Gram-positive and Gram-negative bacteria by ST2-deficient phagocytes. Consistent with a reduced antimicrobial response, phagocytes lacking ST2 displayed a defect in bactericidal activity in response to bacterial challenges with severely impaired phagosome maturation and NOX2 function. Thus, ST2-deficient mice exhibit an increased susceptibility to polymicrobial infection with impaired bacterial clearance, which is associated with defects in phagosome maturation and NOX2-derived production of reactive oxygen species characterized in ST2-deficient phagocytes.
Diseases/Pathways annotated by Medline MESH: Bacterial Infections, Sepsis
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Text Mining Data
TLR2 → ST2: "
ST2 , a member of the Toll/IL-1R superfamily, negatively
regulates both
TLR2 and TLR4 signaling
"
TLR4 → ST2: "
ST2 , a member of the Toll/IL-1R superfamily, negatively regulates both TLR2 and TLR4 signaling
"
Manually curated Databases
No curated data.